AKI

Question 1

Define AKI. (5)

Answer 1

A 50% increase in serum creatinine within 7 days or a urine volume <0.5ml/kg/hr for over 6 hours. Basically an abrupt decline in actual GFR.

Question 2

Describe the epidemiology of AKI. (2)

Answer 2

Present in 5% of hospitalised patients, with an approximately 30% mortality of these.

Question 3

Describe pre-Renal AKI (3)

Answer 3

Actual GFR reduced due to reduced renal blood flow.

No cellular damage, so kidneys work hard to overcome this by reabsorbing salt and water.

Question 4

Describe the changes that occur to maintain GFR in low renal perfusion. (2)

Answer 4

Prostaglandins are high to dilate afferent arteriole, and Angiotensin II is high to constrict efferent arteriole.

Question 5

Describe the effect that drugs can have on GFR in a low perfusion state. (3)

Answer 5

NSAIDs inhibit prostaglandins so stop dilation of afferent.
ACEi or ARBs inhibit Angiotensin II to stop constriction of efferent.
GFR falls.

Question 6

Describe some causes of renal AKI. (8)

Answer 6

Small vessel disease - vasculitis, atheroembolism.
Glormerular disease - lupus, IgA nephropathy, infective endocarditis, Anti-GBM disease.
ATN - ischaemia, nephrotoxins, rhabdomyalsis, radio-contrast agents.
Acute interstitial nephritis - drugs, infection, systemic disease causing eosinophilia.

Question 7

Explain why pre-Renal AKI is reversible.

Answer 7

It occurs in a low volume state, so fluid resuscitation can up the volume and reverse the injury.

Question 8

Define ATN and it’s reversibility. (2)

Answer 8

Acute tubular necrosis that can be caused by ischaemia, nephrotoxins or sepsis (often more than one). Cellular damage means fluid resuscitation can overload rather than help.

Question 9

Describe the differences between ATN and pre-Renal AKI. (3)

Why Is this difference not always acurate? (2)

Answer 9

Pre-Renal: denser urine, high osmolarity, low Na+.
ATN: lighter urine, low osmolarity, high Na+.
Elderly and those on diuretics can’t concentrate urine, so they won’t have high osmolarity or low sodium even if pre-Renal.

Question 10

Define a nephrotoxin. (2)

Give examples of endogenous and exogenous nephrotoxins. (4)

Answer 10

They damage epithelial cells lining tubules causing cell death.
Exogenous: myoglobin, ureteric, bilirubin.
Endogenous: endotoxins from bacterial sepsis, x Ray contrast, drugs (Gentamicin)l poisons (antifreeze).

Question 11

Describe rhabdomyolysis. (3)

Answer 11

Release of myoglobin due to muscle necrosis following a crush injury (actual crush injuries, unconscious drug users, those stuck on the floor). Forms ‘coca-cola’ urine.

Question 12

Describe post-Renal AKI. (4)

Answer 12

Caused by bilateral obstruction (or unilateral with one kidney) with continued urine production causing a rise in intraluminal pressure and hydroureter. Causes hydronephrosis and a decrease in renal function.

Question 13

Describe the investigations of AKI.

Answer 13

Urinanalysis - +++blood or +++protein indicates renal AKI. Culture urine if dipstick positive.
USS - diagnose obstruction. Not needed if pre-Renal is certain.
CXR - pulmonary oedema.

Question 14

Describe the management of AKI. (4)

Explain why diuretics won’t work here. (1)

Answer 14

Volume overload - restrict salt and water (loop diuretics won’t work if there’s been tubular damage).
Hyperkalaemia - calcium gluconate, dextrose + insulin, stop K+ sparing diuretics.
Acidosis - no real treatment.

Question 15

Give 4 simple characteristics of AKI (4)

Answer 15

Big slow raise in creatinine
Fast small raise in creatinine
Decrease in urine output
Decrease in eGFR.